Contrast-induced nephropathy - mechanism
Core concept
- Three mechanisms acting on the same vulnerable segment - the outer medulla
- Medullary hypoxia - contrast triggers renal vasoconstriction (inc endothelin, inc adenosine, dec NO and dec prostaglandins)
- The outer medullary thick ascending limb already runs at a PO2 of ~10-20 mmHg with a high ATP demand
- -> ischaemic tubular injury
- Direct tubular cytotoxicity - contrast is taken up by proximal tubular cells -> oxidative stress, mitochondrial injury, apoptosis, vacuolisation
- Rheological effects - high viscosity and osmolality -> inc tubular fluid viscosity, dec medullary flow, osmotic diuresis
- Medullary hypoxia - contrast triggers renal vasoconstriction (inc endothelin, inc adenosine, dec NO and dec prostaglandins)
- -> the same target as ATN: the outer medullary watershed
- Terminology has changed and the distinction is examinable
- CA-AKI (contrast-associated AKI) = any AKI temporally after contrast - correlation only
- CI-AKI (contrast-induced AKI) = AKI causally attributable to contrast - much rarer
3 more sections, plus exam facts
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